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\author{kjaniskevich}
\pdfinfo{
  /Title (pharm250-nervous-system.pdf)
  /Creator (Cheatography)
  /Author (kjaniskevich)
  /Subject (PHARM250 Nervous system Cheat Sheet)
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        \hspace*{-6pt}\includegraphics[width=5.8cm]{/web/www.cheatography.com/public/images/cheatography_logo.pdf}}
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    \vspace{-2pt}\large{\bf{\textcolor{DarkBackground}{\textrm{PHARM250 Nervous system Cheat Sheet}}}} \\
    \normalsize{by \textcolor{DarkBackground}{kjaniskevich} via \textcolor{DarkBackground}{\uline{cheatography.com/132444/cs/26822/}}}
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  \mymulticolumn{2}{p{5.377cm}}{\bf\textcolor{white}{Cheatographer}}  \\
  \vspace{-2pt}kjaniskevich \\
  \uline{cheatography.com/kjaniskevich} \\
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  \mymulticolumn{1}{p{5.377cm}}{\bf\textcolor{white}{Cheat Sheet}}  \\
   \vspace{-2pt}Published 1st March, 2021.\\
   Updated 1st March, 2021.\\
   Page {\thepage} of \pageref{LastPage}.
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  Measure your website readability!\\
  www.readability-score.com
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\begin{tabularx}{8.4cm}{x{4 cm} x{4 cm} }
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\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Classification of autonomic drugs}}  \tn
% Row 0
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Stimulate parasympathetic nervous system & Cholinergic \{\{nl\}\} parasympathomimetic \{\{nl\}\}or muscarinic agonists \tn 
% Row Count 4 (+ 4)
% Row 1
\SetRowColor{white}
Inhibit parasympathetic nervous system & Anticholinergics\{\{nl\}\}parasympatholytic\{\{nl\}\} or muscarinic blockers \tn 
% Row Count 8 (+ 4)
% Row 2
\SetRowColor{LightBackground}
Stimulate sympathetic nervous system & Adrenergic \{\{nl\}\}sympathomimetics \{\{nl\}\}or adrenergic agonists \tn 
% Row Count 12 (+ 4)
% Row 3
\SetRowColor{white}
Inhibit sympathetic nervous system & Adrenergic antagonists\{\{nl\}\} anti-adrenergics\{\{nl\}\} or adrenergic blockers \tn 
% Row Count 16 (+ 4)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
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\begin{tabularx}{8.4cm}{x{1.596 cm} x{2.964 cm} x{3.04 cm} }
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\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Classes of autonomic drugs}}  \tn
% Row 0
\SetRowColor{LightBackground}
\seqsplit{Cholinergics} & Stimulate the \seqsplit{parasympathetic} nervous system \{\{nl\}\}rest-and-digest\{\{nl\}\}Receptor: Acetylcholine (muscarinic) & 1. Direct acting \{\{nl\}\}2.Indirect acting \tn 
% Row Count 8 (+ 8)
% Row 1
\SetRowColor{white}
\seqsplit{Anticholinergics} & Inhibit the \seqsplit{parasympathetic} nervous system, which induces \seqsplit{fight-or-flight} (sympathetic) &  \tn 
% Row Count 14 (+ 6)
% Row 2
\SetRowColor{LightBackground}
\seqsplit{Adrenergic} & Stimulate the sympathetic nervous system Result depends on type and location of receptor (α or β) & 𝛂1 agonist \{\{nl\}\}𝛂2 agonist \{\{nl\}\}𝛃1 agonist \{\{nl\}\}𝛃2 agonist \{\{nl\}\}Catecholamines \tn 
% Row Count 21 (+ 7)
% Row 3
\SetRowColor{white}
\seqsplit{Adrenergic} \seqsplit{antagonist} & Inhibit sympathetic nervous system Action depends greatly on type of receptor (α or β) & 𝛂1 antagonist 𝛃1 antagonist 𝛃2 antagonist \tn 
% Row Count 27 (+ 6)
\hhline{>{\arrayrulecolor{DarkBackground}}---}
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\begin{tabularx}{8.4cm}{x{3.92 cm} x{4.08 cm} }
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\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Primary neurotransmitters in the CNS}}  \tn
% Row 0
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\mymulticolumn{2}{x{8.4cm}}{The CNS is responsible for our perception, mood, consciousness, behaviour, and cognition  Therefore, drugs influence perception, mood, consciousness, behaviour, and cognition by altering neurotransmitter activity} \tn 
% Row Count 5 (+ 5)
% Row 1
\SetRowColor{white}
Serotonin (5HT) & mood \tn 
% Row Count 6 (+ 1)
% Row 2
\SetRowColor{LightBackground}
GABA & inhibitory \tn 
% Row Count 7 (+ 1)
% Row 3
\SetRowColor{white}
Norepinephrine (NE) & stimulatory \tn 
% Row Count 8 (+ 1)
% Row 4
\SetRowColor{LightBackground}
Dopamine (D) & behaviour \& movement \tn 
% Row Count 9 (+ 1)
% Row 5
\SetRowColor{white}
Glutamate & stimulatory \tn 
% Row Count 10 (+ 1)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
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\begin{tabularx}{8.4cm}{x{2.432 cm} x{2.584 cm} x{2.584 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Adverse effects of CNS drugs}}  \tn
% Row 0
\SetRowColor{LightBackground}
\seqsplit{Benzodiazepine} & drowsiness, sedation, memory loss, weakness, \seqsplit{disorientation}, ataxia, sleep disturbances, hypotension, \seqsplit{blurred/double} vision, nausea and vomiting &  \tn 
% Row Count 12 (+ 12)
% Row 1
\SetRowColor{white}
\seqsplit{Barbiturates} & Rarely prescribed anymore for anxiety or insomnia because of side effects &  \tn 
% Row Count 18 (+ 6)
% Row 2
\SetRowColor{LightBackground}
\seqsplit{Hypnotic/sedatives} & dizziness, headache, daytime drowsiness, dyspepsia, dry mouth, bitter metallic taste, nausea, anterograde amnesia &  \tn 
% Row Count 27 (+ 9)
% Row 3
\SetRowColor{white}
Melatonin & Adverse effects and monitoring mostly limited to drowsiness level (caution with endocrine dysfunction) because it's identical to endogenous &  \tn 
% Row Count 38 (+ 11)
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\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Adverse effects of CNS drugs (cont)}}  \tn
% Row 4
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TCA's & sedation, dizziness, orthostasis, blurred vision, dry mouth, tachycardia, cognitive impairment, constipation, dry eyes, urinary retention &  \tn 
% Row Count 11 (+ 11)
% Row 5
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SSRI's & Transient: headaches, nervousness, insomnia, nausea, diarrhea &  \tn 
% Row Count 16 (+ 5)
% Row 6
\SetRowColor{LightBackground}
 & Long-term: Sexual dysfunction, withdrawal upon \seqsplit{discontinuation} &  \tn 
% Row Count 21 (+ 5)
% Row 7
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MAOI's & : constipation, dry mouth, headaches, changes in heart rate and blood pressure, insomnia, nausea, loss of appetite &  \tn 
% Row Count 30 (+ 9)
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\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Adverse effects of CNS drugs (cont)}}  \tn
% Row 8
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 & Food interactions & foods containing tyramine = Hypertensive Crisis!!! \tn 
% Row Count 4 (+ 4)
% Row 9
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Mood stabilizers & Dizziness, fatigue, short-term memory loss, increased urination, GI upset, dry mouth, muscular weakness, tremors, excessive loss of sodium can lead to toxicity &  \tn 
% Row Count 17 (+ 13)
% Row 10
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 & In the absence of sodium (Na), the cells take in lithium instead &  \tn 
% Row Count 22 (+ 5)
% Row 11
\SetRowColor{white}
 & lithium toxicity & Transient \seqsplit{gastrointestinal} symptoms are the earliest side effects to occur Mild degree of fine tremor of the hands may persist throughout therapy Thirst and polyuria may be followed by increased drowsiness, ataxia, tinnitus and blurred vision, indicating early toxicity  As intoxication progresses the following \seqsplit{manifestations} may occur: confusion, increasing \seqsplit{disorientation}, muscle twitches, \seqsplit{hyperreflexia}, nystagmus, seizures, diarrhea, vomiting, and eventually coma and death \tn 
% Row Count 59 (+ 37)
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\begin{tabularx}{8.4cm}{x{2.432 cm} x{2.584 cm} x{2.584 cm} }
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\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Adverse effects of CNS drugs (cont)}}  \tn
% Row 12
\SetRowColor{LightBackground}
CNS stimulants & Insomnia, anxiety, restlessness, agitation, significant \seqsplit{nausea/vomiting}, anorexia (give with food), Cough, dry mouth, Tachycardia, hypertension, arrhythmias -{}-\textgreater{} monitor and watch for signs of \seqsplit{cardiovascular} disease &  \tn 
% Row Count 17 (+ 17)
% Row 13
\SetRowColor{white}
 & dose in AM or early afternoon &  \tn 
% Row Count 20 (+ 3)
% Row 14
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Typical \seqsplit{antipsychotics} & dizziness, drowsiness, orthostatic hypotension, dry mouth, dry eyes, constipation, blood dyscrasias (abnormal lab tests) &  \tn 
% Row Count 30 (+ 10)
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\begin{tabularx}{8.4cm}{x{2.432 cm} x{2.584 cm} x{2.584 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Adverse effects of CNS drugs (cont)}}  \tn
% Row 15
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 & EPS and NMS occur with typical \seqsplit{antipsychotics} &  \tn 
% Row Count 4 (+ 4)
% Row 16
\SetRowColor{white}
Atypical \seqsplit{antipsychotics} (clozapine) & significant \seqsplit{agranulocytosis}, seizures, tachycardia, NMS • BUT HAS NO EPS &  \tn 
% Row Count 10 (+ 6)
% Row 17
\SetRowColor{LightBackground}
Atypical \seqsplit{antipsychotics} (all the rest) & drowsiness, dizziness, dry mouth, \seqsplit{hyperglycemia}, changes in cholesterol levels, weight gain, EPS &  \tn 
% Row Count 18 (+ 8)
% Row 18
\SetRowColor{white}
\seqsplit{Barbiturates} for seizures & Soft tissue irritant – avoid injecting if possible IM – \seqsplit{inflammation;} IV – tissue necrosis Can cause vitamin deficiencies (D, B12, folate) •	Requires adequate \seqsplit{supplementation} &  \tn 
% Row Count 32 (+ 14)
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\begin{tabularx}{8.4cm}{x{2.432 cm} x{2.584 cm} x{2.584 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Adverse effects of CNS drugs (cont)}}  \tn
% Row 19
\SetRowColor{LightBackground}
Phenytoin & dysrhythmias, headache, nystagmus, confusion, slurred speech, changes urine colour (red/brown), blood dyscrasias, \seqsplit{hyperglycemia}, gingival hypertrophy, skin reactions, osteoporosis &  \tn 
% Row Count 14 (+ 14)
% Row 20
\SetRowColor{white}
Valproic Acid & : sedation, GI upset, prolonged bleeding time, visual disturbances, ataxia, vertigo, muscle weakness, \seqsplit{hepatotoxicity}, pancreatitis, bone marrow suppression &  \tn 
% Row Count 26 (+ 12)
% Row 21
\SetRowColor{LightBackground}
\seqsplit{Succinimides} & mental and physical impairment, psychosis, behavioural changes, CNS effects, bone marrow suppression &  \tn 
% Row Count 34 (+ 8)
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\vfill
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\begin{tabularx}{8.4cm}{x{2.432 cm} x{2.584 cm} x{2.584 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Adverse effects of CNS drugs (cont)}}  \tn
% Row 22
\SetRowColor{LightBackground}
dopamine agonist & reduced impulse control &  \tn 
% Row Count 2 (+ 2)
% Row 23
\SetRowColor{white}
Opioid Analgesics & sedation, fatigue, euphoria, confusion, constipation, respiratory depression, nausea, vomiting &  \tn 
% Row Count 10 (+ 8)
% Row 24
\SetRowColor{LightBackground}
Opioid Antagonist & minimal toxicity, however the effect of reversing analgesia will cause increased blood pressure, tremors, \seqsplit{hyperventilation}, \seqsplit{nausea/vomiting} and drowsiness (i.e. sudden withdrawal symptoms) &  \tn 
% Row Count 25 (+ 15)
% Row 25
\SetRowColor{white}
NSAIDs & gastric and epigastric discomfort, increased bleeding time, nausea, possible \seqsplit{nephrotoxicity}, \seqsplit{cardiovascular} events with long term use &  \tn 
% Row Count 36 (+ 11)
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\begin{tabularx}{8.4cm}{x{2.432 cm} x{2.584 cm} x{2.584 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Adverse effects of CNS drugs (cont)}}  \tn
% Row 26
\SetRowColor{LightBackground}
\seqsplit{acetaminophen} & possible liver damage (hepatotoxic metabolite), causes less gastric irritation than aspirin, does not affect blood coagulation BUT can interact with warfarin &  \tn 
% Row Count 13 (+ 13)
% Row 27
\SetRowColor{white}
Gabapentin & Fatigue, weight gain, heartburn, ataxia, dizziness very common &  \tn 
% Row Count 18 (+ 5)
% Row 28
\SetRowColor{LightBackground}
Pregabalin (Lyrica®) & Dizziness, fatigue, peripheral edema, dry mouth &  \tn 
% Row Count 22 (+ 4)
% Row 29
\SetRowColor{white}
 & better tolerated than Gabapentin &  \tn 
% Row Count 25 (+ 3)
% Row 30
\SetRowColor{LightBackground}
\seqsplit{Corticosteroids} & infections, \seqsplit{hyperglycemia}, hypertension, thinning skin, easy bruising, moon face, osteoporosis, HPA-axis suppression &  \tn 
% Row Count 34 (+ 9)
\end{tabularx}
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\begin{tabularx}{8.4cm}{x{2.432 cm} x{2.584 cm} x{2.584 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Adverse effects of CNS drugs (cont)}}  \tn
% Row 31
\SetRowColor{LightBackground}
Muscle relaxants & sedation, dry mouth, urinary retention \seqsplit{(anticholinergic} effects) &  \tn 
% Row Count 5 (+ 5)
% Row 32
\SetRowColor{white}
Anesthetics & tingling, mucosal irritation, CNS toxicity, \seqsplit{cardiovascular} collapse &  \tn 
% Row Count 11 (+ 6)
% Row 33
\SetRowColor{LightBackground}
Duloxetine \seqsplit{(Cymbalta®)} & Nausea, dizziness, fatigue all common &  \tn 
% Row Count 14 (+ 3)
% Row 34
\SetRowColor{white}
Triptans & dizziness, drowsiness, warming \& prickling sensation, may experience rebound headache \seqsplit{Vasoconstriction}  =↑ BP &  \tn 
% Row Count 23 (+ 9)
% Row 35
\SetRowColor{LightBackground}
Ergot Alkaloids & leg weakness, muscle pain in extremities, nausea and vomiting &  \tn 
% Row Count 28 (+ 5)
\hhline{>{\arrayrulecolor{DarkBackground}}---}
\SetRowColor{LightBackground}
\mymulticolumn{3}{x{8.4cm}}{Serotonin Syndrome \newline ↑ risk when \textgreater{}1 drug that increases serotonin in the body \newline Not always obvious due to promiscuity – triptans, tramadol, etc. \newline symptoms: Hypertension, tremors, sweating, shivering, confusion, anxiety, restlessness, tachycardia, muscle twitching \newline Anywhere from 30 mins after dose -{}-\textgreater{} weeks after dose of the 2nd drug}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}---}
\end{tabularx}
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\begin{tabularx}{8.4cm}{p{0.8 cm} p{0.8 cm} }
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\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Emotional \& Mood Disorders}}  \tn
% Row 0
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\mymulticolumn{2}{x{8.4cm}}{} \tn 
% Row Count 0 (+ 0)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{8.4cm}}{Depression \newline Mood Disorders (Bipolar) \newline Post-traumatic Stress Disorder (PTSD) \newline Attention Deficit Hyperactivity Disorder (ADHD)  \newline Many more (hundreds)}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
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\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Medication for Emotional \& Mood Disorders}}  \tn
% Row 0
\SetRowColor{LightBackground}
{\bf{Antidepressants}} & {\bf{1.Tricyclic antidepressants (TCAs)}} & Work by inhibiting reuptake of norepinephrine, serotonin, and dopamine, leaves more \seqsplit{neurotransmitter} within cleft \tn 
% Row Count 8 (+ 8)
% Row 1
\SetRowColor{white}
 & {\emph{-triptyline; -pramine -oxepine}} &  \tn 
% Row Count 10 (+ 2)
% Row 2
\SetRowColor{LightBackground}
 & {\bf{2.Selective serotonin inhibiters \{\{nl\}\} (SSRIs)}} & Work by inhibiting reuptake of serotonin only \tn 
% Row Count 14 (+ 4)
% Row 3
\SetRowColor{white}
 & {\emph{Citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline}} &  \tn 
% Row Count 19 (+ 5)
% Row 4
\SetRowColor{LightBackground}
 & {\bf{3. Monoamine oxidase inhibitors (MAOIs)}} & Reserved for people who haven't responded to SSRI or TCA\{\{nl\}\}Inhibits monoamine oxidase (MAO) which breaks down norepinephrine leaves more norepinephrine in the synaptic cleft\{\{nl\}\}breaks down dopamine, epinephrine, and serotonin leaves more of these \seqsplit{neurotransmitters} as well causing many side effects and interactions \tn 
% Row Count 40 (+ 21)
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\begin{tabularx}{8.4cm}{x{1.52 cm} x{3.04 cm} x{3.04 cm} }
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\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Medication for Emotional \& Mood Disorders (cont)}}  \tn
% Row 5
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 & {\emph{Phenelzine, tranylcypromine, moclobemide}} &  \tn 
% Row Count 3 (+ 3)
% Row 6
\SetRowColor{white}
 & {\bf{4. Atypical antidepressants}} & Inhibiting reuptake of serotonin, norepinephrine and dopamine activity with different affinities Also work on other receptors like histamine \tn 
% Row Count 12 (+ 9)
% Row 7
\SetRowColor{LightBackground}
 & {\emph{Bupropion (Wellbutrin®, Zyban®)(NDRI), mirtazapine \seqsplit{(Remeron®)(SNRI)}, venlafaxine \seqsplit{(Effexor®)(SNRI)}, duloxetine \seqsplit{(Cymblata®)(SNRI)}, trazodone (Desryl®)(SARI)}} &  \tn 
% Row Count 23 (+ 11)
% Row 8
\SetRowColor{white}
{\bf{Mood stabilizers}} & Work by altering sodium transport across cell membranes By altering sodium transport, it influences the release, synthesis, and reuptake of multiple \seqsplit{neurotransmitters} &  \tn 
% Row Count 34 (+ 11)
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\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Medication for Emotional \& Mood Disorders (cont)}}  \tn
% Row 9
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 & Primarily used for bipolar disorder \seqsplit{(manic-depression)} &  \tn 
% Row Count 4 (+ 4)
% Row 10
\SetRowColor{white}
 & Lithium carbonate &  \tn 
% Row Count 6 (+ 2)
% Row 11
\SetRowColor{LightBackground}
 & \seqsplit{Anticonvulsants:} carbamazepine, divalproex, lamotrigine, valproic acid, gabapentin, topiramate & Anticonvulsants are also used as mood stabilizers because they also alter transport of ions across cell membranes \tn 
% Row Count 14 (+ 8)
% Row 12
\SetRowColor{white}
CNS \seqsplit{stimulants} & Work by heightening awareness and increasing focus (non-specifically)\{\{nl\}\}Primarily used for ADHD in children and adults\{\{nl\}\}All cause an increase in attentiveness and heightened awareness by influencing NE and D release somehow &  \tn 
% Row Count 29 (+ 15)
% Row 13
\SetRowColor{LightBackground}
 & {\emph{Methylphenidate (Ritalin®, Concerta®, Biphentin®) \seqsplit{Dextroamphetamine} (Dexedrine®) \seqsplit{Dextroamphetamine} and amphetamine (Adderall®) \seqsplit{Lisdexamfetamine} (Vyvanse®)}} &  \tn 
% Row Count 40 (+ 11)
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\begin{tabularx}{8.4cm}{x{3.68 cm} x{4.32 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Degenerative diseases}}  \tn
% Row 0
\SetRowColor{LightBackground}
{\bf{Parkinson's \{\{nobreak\}\}disease}} & Gradual destruction of neurons from substantia nigra → striatum of brain that use dopamine to communicate \{\{nl\}\} Movements and impulses essential to performance of movements  \{\{nl\}\}↓ number of dopaminergic neurons → ↓ dopamine \{\{nl\}\}Symptoms are a characterization of ↓ dopamine \tn 
% Row Count 14 (+ 14)
% Row 1
\SetRowColor{white}
Parkinson's symptoms & Classic features:\{\{nl\}\}Tremor, Bradykinesia, Rigidity, Loss of balance\{\{nl\}\}Other features;\{\{nl\}\}Depression, anxiety, mood change, Memory loss -{}-\textgreater{} dementia, Difficulty concentrating, Change in sense of smell, Change in sleeping patterns, Constipation, light-headedness, sweaty, Difficulty swallowing, chewing, speaking, blinking \tn 
% Row Count 30 (+ 16)
\end{tabularx}
\par\addvspace{1.3em}

\vfill
\columnbreak
\begin{tabularx}{8.4cm}{x{3.68 cm} x{4.32 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Degenerative diseases (cont)}}  \tn
% Row 2
\SetRowColor{LightBackground}
{\bf{Dementia}} & A term that describes a decline in a variety of functions (e.g. memory, language, motor activities, ability to recognize or identify objects, complex decision-making) which eventually causes a person to have difficulty performing everyday activities \tn 
% Row Count 12 (+ 12)
% Row 3
\SetRowColor{white}
\mymulticolumn{2}{x{8.4cm}}{{\bf{Types of Dementia }}} \tn 
% Row Count 13 (+ 1)
% Row 4
\SetRowColor{LightBackground}
Alzheimer's Disease & amyloid plaques and tangles \tn 
% Row Count 15 (+ 2)
% Row 5
\SetRowColor{white}
Vascular Dementia & reduced blood supply \tn 
% Row Count 16 (+ 1)
% Row 6
\SetRowColor{LightBackground}
Frontotemporal Dementia & younger patients, highly genetic, odd behaviours \tn 
% Row Count 19 (+ 3)
% Row 7
\SetRowColor{white}
Lewy Body Dementia & presence of Lewy Bodies, well-formed hallucinations \tn 
% Row Count 22 (+ 3)
% Row 8
\SetRowColor{LightBackground}
Parkinson's Disease Dementia & Parkinson's usually diagnosed first – both neurodegenerative \tn 
% Row Count 26 (+ 4)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{8.4cm}}{Parkinson's disease management: All pharmacotherapy focuses on ↑ dopamine levels (directly or indirectly)}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
\par\addvspace{1.3em}

\begin{tabularx}{8.4cm}{x{3.28 cm} x{4.72 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Classes of medication for Parkinson's}}  \tn
% Row 0
\SetRowColor{LightBackground}
Levodopa & Effective cornerstone of therapy\{\{nl\}\}  Dopamine cannot cross blood-brain barrier (BBB) The enzyme that creates dopamine (decarboxylase) is everywhere in the body\{\{nl\}\}  Levodopa → crosses BBB → converted to dopamine via decarboxylase\{\{nl\}\} It is a prodrug\{\{nl\}\}Levodopa is always paired with either carbidopa or benserazide (decarboxylase inhibitors that DO NOT cross BBB), \{\{nl\}\}which does two things:\{\{nl\}\}  1) Enhances distribution to brain\{\{nl\}\} 2) Minimizes acute side effects Because conversion to dopamine occurring past BBB (mostly) \tn 
% Row Count 24 (+ 24)
% Row 1
\SetRowColor{white}
Dopamine Agonists & stimulate dopamine receptors \tn 
% Row Count 26 (+ 2)
% Row 2
\SetRowColor{LightBackground}
MAO-B Inhibitors (MAOIs) & inhibit the enzyme that breaks down dopamine \tn 
% Row Count 28 (+ 2)
% Row 3
\SetRowColor{white}
Amantadine & either releases more dopamine or inhibits re-uptake of dopamine (exact mechanism unknown) \{\{nl\}\}{\emph{also anti-viral}} \tn 
% Row Count 33 (+ 5)
\end{tabularx}
\par\addvspace{1.3em}

\vfill
\columnbreak
\begin{tabularx}{8.4cm}{x{3.28 cm} x{4.72 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Classes of medication for Parkinson's (cont)}}  \tn
% Row 4
\SetRowColor{LightBackground}
COMT Inhibitors & inhibit peripheral conversion of levodopa to dopamine (making levodopa more efficient) \tn 
% Row Count 4 (+ 4)
% Row 5
\SetRowColor{white}
\seqsplit{Anticholinergics} \{\{nobreak\}\} & block acetylcholine, which restores balance of acetylcholine and dopamine \{\{nl\}\}for tremor only \tn 
% Row Count 9 (+ 5)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{8.4cm}}{All other medications for Parkinson's (excluding Levodopa) work to either directly or indirectly to↑ dopamine in brain}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
\par\addvspace{1.3em}

\begin{tabularx}{8.4cm}{x{4 cm} x{4 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Classes of medication for Dementia}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{8.4cm}}{{\bf{Treatment of Dementia}}} \tn 
% Row Count 1 (+ 1)
% Row 1
\SetRowColor{white}
1.Cholinesterase Inhibitors \{\{nl\}\}{\emph{Donepezil, galantamine, rivastigmine}} & Prevent breakdown of acetylcholine (Theory: lack of acetylcholine causes plaques \& tangles) \{\{nl\}\} May show small improvements in measures of cognition and activities of daily living (ADL) (1-3 points on MMSE) \{\{nl\}\} May slow progression (by months, not years)\{\{nl\}\} If benefit, seen in 3-6 months  \{\{nl\}\} Only approved for Alzheimer's but prescribed for all types \tn 
% Row Count 20 (+ 19)
% Row 2
\SetRowColor{LightBackground}
\seqsplit{2.N-methyl-D-aspartate} (NMDA) antagonist\{\{nl\}\}{\emph{Memantine}} & Block glutamate (excitatory amino acid) at NMDA receptor (Theory: persistent activation of NMDA contributes to symptoms) \{\{nl\}\} No effect on acetylcholine\{\{nl\}\} Alone or in combo with cholinesterase inhibitor – directly conflicting evidence re: benefit \{\{nl\}\} Indication: Moderate → Severe Alzheimer's\{\{nl\}\} Renally excreted (dosage adjustment needed for impairment) \tn 
% Row Count 39 (+ 19)
\end{tabularx}
\par\addvspace{1.3em}

\vfill
\columnbreak
\begin{tabularx}{8.4cm}{x{4 cm} x{4 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Classes of medication for Dementia (cont)}}  \tn
% Row 3
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{8.4cm}}{{\bf{Management of Behavioural \& Psychological Symptoms of Dementia (BPSD)}}} \tn 
% Row Count 2 (+ 2)
% Row 4
\SetRowColor{white}
\mymulticolumn{2}{x{8.4cm}}{Antipsychotics, benzodiazepines, antidepressants, stimulants and more} \tn 
% Row Count 4 (+ 2)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
\par\addvspace{1.3em}

\begin{tabularx}{8.4cm}{x{3.04 cm} x{4.96 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Classification of Pain}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{8.4cm}}{{\bf{Duration}}} \tn 
% Row Count 1 (+ 1)
% Row 1
\SetRowColor{white}
A.Acute pain & Intense, Less than 6 months\{\{nl\}\} E.g. sprained ankle \tn 
% Row Count 4 (+ 3)
% Row 2
\SetRowColor{LightBackground}
B. Chronic pain & Persists for longer than 6 months, Interferes with daily activities, Associated with feelings of hopelessness\{\{nl\}\} E.g. permanent nerve injury \tn 
% Row Count 10 (+ 6)
% Row 3
\SetRowColor{white}
\mymulticolumn{2}{x{8.4cm}}{{\bf{Source}}} \tn 
% Row Count 11 (+ 1)
% Row 4
\SetRowColor{LightBackground}
A. Nociceptor \{\{nobreak\}\} & Pain Due to injury to tissues \{\{nl\}\} Sharp, localized; or Dull, throbbing, aching \{\{nl\}\} E.g. paper cut, broken bones \tn 
% Row Count 16 (+ 5)
% Row 5
\SetRowColor{white}
B. Neuropathic Pain & Due to injury to nerves \{\{nl\}\} Burning, shooting, numbing\{\{nl\}\} E.g. nerve injury, shingles \tn 
% Row Count 20 (+ 4)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{8.4cm}}{Pharmacological management  \newline Requires thorough: \newline Health history (including allergies) \newline BPMH – best possible medication history \newline Includes an assessment of stress, coping mechanisms, potential for dependency \newline Baseline assessment including character, location, duration and intensity of pain}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
\par\addvspace{1.3em}

\begin{tabularx}{8.4cm}{x{3.12 cm} x{4.88 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Migraines}}  \tn
% Row 0
\SetRowColor{LightBackground}
Goal of treatment & To reduce acute pain via\{\{nl\}\} 1.Triptans or\{\{nl\}\} 2.Ergot alkaloids \tn 
% Row Count 3 (+ 3)
% Row 1
\SetRowColor{white}
 & To prevent further migraines from occurring\{\{nl\}\} If patient experiences a significant amount of migraines\{\{nl\}\} β-blockers, anticonvulsants (topiramate, valproic acid), calcium channel blockers, TCAs, venlafaxine \tn 
% Row Count 12 (+ 9)
% Row 2
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{8.4cm}}{Classes of drugs for migraines} \tn 
% Row Count 13 (+ 1)
% Row 3
\SetRowColor{white}
{\bf{1.Triptans}} \{\{nobreak\}\} & Selective serotonin receptor agonist on intracranial blood vessels and sensory nerves on the trigeminal system\{\{nl\}\} Causes vasoconstriction and reduces neurogenic inflammation, relieving migraine headache \{\{nl\}\} Used for acute cluster headaches or migraines (with or without aura) as early as possible \{\{nl\}\} Available as regular oral tabs, oral disintegrating tablets, injections, nasal spray (due to frequent nausea/vomiting) – we want quick onset \{\{nl\}\} Expensive (require EDS in Sask)\{\{nl\}\}Interaction with any other drug that also ↑ serotonin  serotonin syndrome \{\{nl\}\}Tolerance can develop – remind patients to use only when necessary and as few doses as needed \tn 
% Row Count 42 (+ 29)
\end{tabularx}
\par\addvspace{1.3em}

\vfill
\columnbreak
\begin{tabularx}{8.4cm}{x{3.12 cm} x{4.88 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Migraines (cont)}}  \tn
% Row 4
\SetRowColor{LightBackground}
{\bf{2.Ergot alkaloids}} & Serotonin receptor agonist and interacts with dopamine and adrenergic receptors (α-blocker) \{\{nl\}\} Therefore, more adverse effects\{\{nl\}\} Dihydroergotamine – given IV, may see repeated administration for 3-7 days to break cycle of repeat migraines\{\{nl\}\} DO NOT GIVE WITHIN 24 HOURS OF TRIPTAN\{\{nl\}\} Additive vasoconstriction -{}-\textgreater{} coronary vasospasm\{\{nl\}\} Mostly used if triptans fail \tn 
% Row Count 16 (+ 16)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{8.4cm}}{Migraine Monitoring: \newline History of migraines, triggers, and previous treatment, focus on prevention \newline Effectiveness of treatment (assess pain level) \newline Blood pressure and pulse \newline Watch for chest pain, palpitations, confusion, tingling in extremities, or sudden change of headache status (Fever? Rash? Stiff neck?) \newline Headaches are usually a symptom}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
\par\addvspace{1.3em}

\begin{tabularx}{8.4cm}{x{2.736 cm} x{1.976 cm} x{2.888 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Nervous system}}  \tn
% Row 0
\SetRowColor{LightBackground}
Branches of peripheral nervous system & 1.Somatic nervous system & Voluntary control over skeletal muscles \tn 
% Row Count 3 (+ 3)
% Row 1
\SetRowColor{white}
 & 2. Autonomic nervous system & Involuntary control over smooth and cardiac muscle and glands Divided into sympathetic and \seqsplit{parasympathetic} \tn 
% Row Count 11 (+ 8)
% Row 2
\SetRowColor{LightBackground}
Autonomic nervous system & 1. \seqsplit{Sympathetic} & Activated under stress  \seqsplit{Fight-or-flight} response Primitive response to avoid harm \tn 
% Row Count 17 (+ 6)
% Row 3
\SetRowColor{white}
 & 2. \seqsplit{Parasympathetic} & Activated under non-stressful conditions  \seqsplit{Rest-and-digest} response \tn 
% Row Count 22 (+ 5)
\hhline{>{\arrayrulecolor{DarkBackground}}---}
\end{tabularx}
\par\addvspace{1.3em}

\begin{tabularx}{8.4cm}{x{1.596 cm} x{2.66 cm} x{3.344 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Primary neurotransmitters in the periphery}}  \tn
% Row 0
\SetRowColor{LightBackground}
\seqsplit{Norepinephrine} (NE) & Binds with adrenergic receptors &  \tn 
% Row Count 3 (+ 3)
% Row 1
\SetRowColor{white}
 & Alpha (α) receptors (α1 \& α2) & α1-adrenergic Receptors In sympathetic target organs except heart \{\{nl\}\}α2-adrenergic Receptors At presynaptic adrenergic neuron terminals \tn 
% Row Count 12 (+ 9)
% Row 2
\SetRowColor{LightBackground}
 & Beta (β) receptors (β1 \& β2) & β1-adrenergic Receptors Mostly in heart muscle \{\{nl\}\}β2-adrenergic Receptors Mostly in the lungs \tn 
% Row Count 18 (+ 6)
% Row 3
\SetRowColor{white}
\seqsplit{Acetylcholine} (Ach) & Binds with cholinergic receptors &  \tn 
% Row Count 21 (+ 3)
% Row 4
\SetRowColor{LightBackground}
 & Muscarinic receptors & Binding to muscarinic receptor varies between stimulatory and inhibitory action, depending on site \tn 
% Row Count 27 (+ 6)
% Row 5
\SetRowColor{white}
 & Nicotinic receptors & Skeletal muscle, smooth muscle, glands \{\{nl\}\} Not many useful drugs affect nicotinic receptors \tn 
% Row Count 33 (+ 6)
\hhline{>{\arrayrulecolor{DarkBackground}}---}
\end{tabularx}
\par\addvspace{1.3em}

\begin{tabularx}{8.4cm}{x{3.76 cm} x{4.24 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Adverse effects of autonomic drugs}}  \tn
% Row 0
\SetRowColor{LightBackground}
Cholinergics & salivation, sweating, abdominal cramping and hypotension \tn 
% Row Count 3 (+ 3)
% Row 1
\SetRowColor{white}
Anticholinergics \{\{nobreak\}\} & dry mouth, constipation, urinary retention, confusion, tachycardia\{\{nl\}\} Less mucous production = dry mouth, eyes, nose \{\{nl\}\}Pupil dilation, blurred/double vision, increased intraocular pressure \{\{nl\}\}Less sweating  = ↑ in body temp\{\{nl\}\}Urinary retention = ↑ risk of infection\{\{nl\}\}CNS = Agitation, inability to concentrate, confusion -\textgreater{} delirium, hallucinations, illogical thinking, incoherent speech \tn 
% Row Count 23 (+ 20)
% Row 2
\SetRowColor{LightBackground}
α-adrenergics & Oral - anxiety, restlessness, tremor, hypertension, tachycardia\{\{nl\}\}Nasal – burning of mucosa, rebound congestion if used for long periods \tn 
% Row Count 30 (+ 7)
\end{tabularx}
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\vfill
\columnbreak
\begin{tabularx}{8.4cm}{x{3.76 cm} x{4.24 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Adverse effects of autonomic drugs (cont)}}  \tn
% Row 3
\SetRowColor{LightBackground}
adrenergic antagonist β1 -blocking & bradycardia, hypotension, headache, fatigue, dizziness, sleep disturbances, nausea; most are dose-related and appear early in therapy Rebound tachycardia, arrhythmias and infarction if discontinued suddenly \tn 
% Row Count 10 (+ 10)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{8.4cm}{x{2.4 cm} x{5.6 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Anxiety and Sleep Disorders}}  \tn
% Row 0
\SetRowColor{LightBackground}
Anxiety Disorders & Generalized anxiety disorder (GAD) ,Phobias, Panic disorders, Obsessive-compulsive disorder (OCD), Post-traumatic stress disorder (PTSD) \tn 
% Row Count 5 (+ 5)
% Row 1
\SetRowColor{white}
Sleep Disorders & Either an inability to: Fall asleep, Stay asleep, or  Both \tn 
% Row Count 8 (+ 3)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{8.4cm}}{In both anxiety and sleep disorders, nonpharmacological management is more effective LONG TERM \newline  \newline Medications provide relief but should be used for SHORT TERM if possible in addition to non-pharmacological management}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
\par\addvspace{1.3em}

\begin{tabularx}{8.4cm}{x{3.36 cm} x{4.64 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{CNS depressants}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{8.4cm}}{} \tn 
% Row Count 0 (+ 0)
% Row 1
\SetRowColor{white}
\seqsplit{1.Benzodiazepines} & Intensify GABA (bind to benzodiazepine receptors on a GABA receptor) \tn 
% Row Count 3 (+ 3)
% Row 2
\SetRowColor{LightBackground}
2.Barbiturates & Enhance GABA (bind to barbiturate receptor on GABA receptor) \tn 
% Row Count 6 (+ 3)
% Row 3
\SetRowColor{white}
\seqsplit{3.Hypnotics/Sedatives} & Commonly also use a benzodiazepine receptor to potentiate GABA, but much more specific \tn 
% Row Count 10 (+ 4)
% Row 4
\SetRowColor{LightBackground}
 & Bind only to GABA1 for sleep Only cause sedation no anxiolytic or anticonvulsant properties \tn 
% Row Count 14 (+ 4)
% Row 5
\SetRowColor{white}
4.Miscellaneous & Can act on any neurotransmitter any drug that causes sedation can potentially be used to induce or prolong sleep even if it is an adverse effect \tn 
% Row Count 21 (+ 7)
% Row 6
\SetRowColor{LightBackground}
 & Includes antihistamines such as diphenhydramine (Benadryl®), dimenhydrinate (Gravol®) or hydroxyzine (Atarax®) \tn 
% Row Count 26 (+ 5)
% Row 7
\SetRowColor{white}
CNS depression is a continuum & muscle relaxation\textgreater{}sedation\textgreater{}induce sleep\textgreater{}anesthesia\textgreater{}coma\textgreater{}death \tn 
% Row Count 29 (+ 3)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{8.4cm}}{Slow down neural activity in the brain, May or may not be specific for certain neurotransmitters}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
\par\addvspace{1.3em}

\begin{tabularx}{8.4cm}{x{3.04 cm} x{3.8 cm} p{0.76 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Classes of Medication for Psychosis}}  \tn
% Row 0
\SetRowColor{LightBackground}
{\bf{Typical antipsychotics}}\{\{nobreak\}\} & conventional, 1st generation \{\{nl\}\}- good at managing positive symptoms, \{\{nl\}\}no dependence \{\{nl\}\}D \textgreater{} 5HT\{\{nl\}\} More side effects (especially EPS) than atypical &  \tn 
% Row Count 9 (+ 9)
% Row 1
\SetRowColor{white}
A. Phenothiazines \{\{nl\}\}{\bf{Chlorpromazine}} & Blocks post-synaptic dopamine receptors; also blocks histamine and muscarinic receptors \{\{nl\}\} Used to manage mania and psychosis, prevention and treatment of nausea and vomiting &  \tn 
% Row Count 18 (+ 9)
% Row 2
\SetRowColor{LightBackground}
\mymulticolumn{3}{x{8.4cm}}{other \seqsplit{phenothiazines:Fluphenazine}, Methotrimeprazine, Perphenazine, Promazine, Trifluoperazine} \tn 
% Row Count 20 (+ 2)
% Row 3
\SetRowColor{white}
B. \seqsplit{Non-Phenothiazines} \{\{nl\}\}{\bf{Haloperidol}} & Blocks post-synaptic dopamine receptors \{\{nl\}\} Used to manage psychotic disorders, Tourette's, manic states; also an antiemetic &  \tn 
% Row Count 27 (+ 7)
% Row 4
\SetRowColor{LightBackground}
\mymulticolumn{3}{x{8.4cm}}{other non-phenothiazines: Flupentixol, Loxapine, Pimozide, Thiothixene, Zuclopenthixol} \tn 
% Row Count 29 (+ 2)
% Row 5
\SetRowColor{white}
{\bf{Atypical anti-psychotics}} \{\{nobreak\}\} & unconventional, 2nd generation \{\{nl\}\}Newer class – now drugs of choice\{\{nl\}\} No dependence\{\{nl\}\} More specific for serotonin than dopamine receptors, with different affinities\{\{nl\}\} Also bind to α-receptors in periphery \{\{nl\}\}Less side effects (especially EPS) than typicals/1st Gen &  \tn 
% Row Count 44 (+ 15)
\end{tabularx}
\par\addvspace{1.3em}

\vfill
\columnbreak
\begin{tabularx}{8.4cm}{x{3.04 cm} x{3.8 cm} p{0.76 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{3}{x{8.4cm}}{\bf\textcolor{white}{Classes of Medication for Psychosis (cont)}}  \tn
% Row 6
\SetRowColor{LightBackground}
A.Clozapine & Blocks dopamine receptors; also blocks serotonin, muscarinic, and histamine receptors  Reserved only for treatment-resistant schizophrenia because of adverse effects\{\{nl\}\} does not have EPS &  \tn 
% Row Count 10 (+ 10)
% Row 7
\SetRowColor{white}
B. Quetiapine (Seroquel®) & Blocks serotonin receptors; also slightly blocks dopamine receptors \{\{nl\}\} Used to treat schizophrenia and bipolar disorder; also used in the behavioural and psychological symptoms of dementia (BPSD) &  \tn 
% Row Count 20 (+ 10)
% Row 8
\SetRowColor{LightBackground}
\mymulticolumn{3}{x{8.4cm}}{Others atypicals:Olanzapine (Zyprexa®) Risperidone (Risperdal®) Paliperidone (Invega®) Ziprasidone (Zeldox®)} \tn 
% Row Count 23 (+ 3)
% Row 9
\SetRowColor{white}
\mymulticolumn{3}{x{8.4cm}}{{\bf{Miscellaneous}}} \tn 
% Row Count 24 (+ 1)
% Row 10
\SetRowColor{LightBackground}
A.Aripiprazole (Abilify®) & Partial dopamine and serotonin agonist; also serotonin antagonist at other sites\{\{nl\}\} Used for schizophrenia, bipolar, and depression (as an add-on)\{\{nl\}\} Fewer side effects but not as effective as others\{\{nl\}\}   Will also see combinations of antidepressants, mood stabilizers, and benzodiazepines &  \tn 
% Row Count 39 (+ 15)
\hhline{>{\arrayrulecolor{DarkBackground}}---}
\SetRowColor{LightBackground}
\mymulticolumn{3}{x{8.4cm}}{Antipsychotics are not a cure for schizophrenia – but they are effective if continued  \newline Medications are only effective for as long as the client takes the medication – no dependence \newline They often have multiple undesirable side effects: \newline Agranulocytosis, EPS, weight gain, sedation, dyskinesias, anticholinergic effects \newline Effectiveness can lead to discontinuation}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}---}
\end{tabularx}
\par\addvspace{1.3em}

\begin{tabularx}{8.4cm}{x{2.48 cm} x{5.52 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Seizure disorders}}  \tn
% Row 0
\SetRowColor{LightBackground}
Seizure & a disturbance of electrical activity in the brain that can affect consciousness, motor activity, and sensation\{\{nl\}\} Not every seizure consists of convulsions\{\{nl\}\} Many types starting with local (one section) or generalized (whole brain) \tn 
% Row Count 9 (+ 9)
% Row 1
\SetRowColor{white}
Convulsions & involuntary, violent spasms of the large skeletal muscles of face, neck, arms, and legs \tn 
% Row Count 13 (+ 4)
% Row 2
\SetRowColor{LightBackground}
Epilepsy & a disorder characterized by recurrent seizures \{\{nl\}\} Those seizures can be any type \{\{nl\}\} You can experience a seizure without having epilepsy \tn 
% Row Count 19 (+ 6)
% Row 3
\SetRowColor{white}
Causes of seizures & Infectious diseases \{\{nl\}\} Trauma to head\{\{nl\}\} Metabolic disorders like dehydration, hypoglycemia, kidney disease, electrolyte imbalances \{\{nl\}\} Vascular diseases causing lack of oxygen\{\{nl\}\} Pediatric disorders febrile seizures\{\{nl\}\} Tumours \tn 
% Row Count 28 (+ 9)
% Row 4
\SetRowColor{LightBackground}
Seizure Threshold & the balance between excitatory and inhibitory forces in the brain which affect how susceptible a person is to seizures \{\{nl\}\}Important: many drugs that alter CNS activity can lower the seizure threshold – this leads to many potential drug interactions \tn 
% Row Count 38 (+ 10)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
\par\addvspace{1.3em}

\begin{tabularx}{8.4cm}{x{4 cm} x{4 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Classes of Medication for seizure disorders}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{8.4cm}}{{\bf{Drugs that potentiate GABA}}} \tn 
% Row Count 1 (+ 1)
% Row 1
\SetRowColor{white}
a.Barbiturates \{\{nobreak\}\} & Potentiate GABA (inhibitory) and suppress the firing ability of neurons by stimulating an influx of Cl- \{\{nl\}\}  CNS depressants \{\{nl\}\} Takes several weeks for control\{\{nl\}\} May be used as monotherapy \tn 
% Row Count 11 (+ 10)
% Row 2
\SetRowColor{LightBackground}
{\emph{Phenobarbital}} & Causes least sedation\{\{nl\}\}Follows CNS depression spectrum \{\{nl\}\}Dependence and withdrawal occur \tn 
% Row Count 16 (+ 5)
% Row 3
\SetRowColor{white}
b.Benzodiazepines \{\{nobreak\}\} & Intensify GABA by binding to benzodiazepine receptors, which stimulates an influx of Cl- \{\{nl\}\} Work very quickly if injected (used in status epilepticus) \{\{nl\}\} Usually an adjunct to other drugs because of dependence and tolerance – reason to use short-term only\{\{nl\}\} Follow CNS depression spectrum \tn 
% Row Count 32 (+ 16)
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\begin{tabularx}{8.4cm}{x{4 cm} x{4 cm} }
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\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Classes of Medication for seizure disorders (cont)}}  \tn
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{\emph{Diazepam}} & As an anti-convulsant, used for short-term seizure control, calming and relaxation \tn 
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c.Miscellaneous & {\emph{Primidone}} – some classify as a barbiturate\{\{nl\}\}  {\emph{Topiramate}} – a combo of mechanisms (blocks Na+ influx, enhances GABA at some receptors - different from benzodiazepines, and more) \tn 
% Row Count 15 (+ 10)
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\mymulticolumn{2}{x{8.4cm}}{{\bf{Drugs that suppress Na+ influx}}} \tn 
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 & Desensitize Na+ channels, which prevents influx of Na+ (different from blocking or antagonizing)\{\{nl\}\} Sodium movement is a main factor that determines whether neuron will undergo an action potential (excitation)\{\{nl\}\} No dependence or tolerance\{\{nl\}\} Not all require lab monitoring\{\{nl\}\} In CNS action potentials Na+ \textgreater{} Ca+ \tn 
% Row Count 33 (+ 17)
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\begin{tabularx}{8.4cm}{x{4 cm} x{4 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Classes of Medication for seizure disorders (cont)}}  \tn
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a.Hydantoins \{\{nl\}\}{\emph{({\bf{phenytoin}} and fosphenytoin)}} & Very common, treats many types of seizures \{\{nl\}\} Very narrow therapeutic range – requires monitoring\{\{nl\}\}LOTS of drug interactions with anticoagulants, corticosteroids, supplements; impairs oral contraceptives and some antibiotics \tn 
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b.Miscellaneous (phenytoin-like) \{\{nl\}\} {\emph{carbamazepine, lamotrigine, {\bf{valproic acid}} (\& divalproex}})\{\{nl\}\} & Still desensitizes sodium channels, which prevents influx of Na+ \{\{nl\}\}Used for absence and mixed-type seizures \tn 
% Row Count 18 (+ 6)
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\mymulticolumn{2}{x{8.4cm}}{{\bf{Drugs that suppress Ca+ influx}}} \tn 
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a.Succinimides\{\{nl\}\}{\emph{Ethosuximide and methsuximide}} & Block calcium channels, which delays Ca+ influx, which depresses the activity of neurons in the motor cortex \{\{nl\}\} Calcium influx is not as dominant as sodium influx \{\{nl\}\}In CNS action potentials Na+ \textgreater{} Ca+ \tn 
% Row Count 30 (+ 11)
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\begin{tabularx}{8.4cm}{x{4 cm} x{4 cm} }
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\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Classes of Medication for seizure disorders (cont)}}  \tn
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b. Gabapentin & – unknown mechanism for anticonvulsant activity \{\{nl\}\} Is shaped like GABA (hence the name), but does NOT bind to GABA receptors \{\{nl\}\} Binds to calcium channels to reduce calcium influx\{\{nl\}\} Used mostly for neuropathic pain and migraines now \tn 
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\mymulticolumn{2}{x{8.4cm}}{We use drugs that can: \newline a.Stimulate an influx of Cl- ions, which potentiates GABA \newline b.Delay an influx of Na+ \newline c.Delay an influx of Ca+ \newline In CNS action potentials Na+ \textgreater{} Ca+}  \tn 
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\end{tabularx}
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\begin{tabularx}{8.4cm}{x{4 cm} x{4 cm} }
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\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Drug Classes for Pain}}  \tn
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\mymulticolumn{2}{x{8.4cm}}{{\bf{Analgesics}}} \tn 
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{\bf{a.Opioid analgesics}} & Work in spinal cord and brain (CNS) to alter perception of pain \{\{nl\}\} Moderate to severe pain\{\{nl\}\} Some used for anesthesia\{\{nl\}\} Different levels of potency/efficacy – all are compared to morphine (Gold Standard) \tn 
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Routes for administration & Oral: Systemic effects all over the body at opioid receptors \{\{nl\}\} Parenteral: Localized or systemic – depends how we do it \tn 
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{\emph{Morphine}} & Routes: PO, IV, IM, SC, rectal, epidural, intrathecal \{\{nl\}\} Remember – 5mg PO ǂ 5mg IV\{\{nl\}\}  Duration of action:\{\{nl\}\} PO – 4 to 7h\{\{nl\}\} IV – 4 to 5h\{\{nl\}\} Epidural – 4 to 24h \tn 
% Row Count 29 (+ 10)
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Opioid dependency & Physical dependence lasts 7 days\{\{nl\}\} Psychological dependence can last many months or years\{\{nl\}\} Often, patients switch from IV and inhalation forms to oral form called methadone \tn 
% Row Count 39 (+ 10)
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\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Drug Classes for Pain (cont)}}  \tn
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{\emph{Methadone}} & A long lasting opioid that avoids withdrawal symptoms by stimulating receptors, with no euphoria \{\{nl\}\} Has a long t$\frac{1}{2}$ - most only need to dose once daily (still patient variation) \tn 
% Row Count 9 (+ 9)
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opioid antagonist \{\{nl\}\} {\emph{Naloxone and naltrexone}} & Competitively binds to and blocks mu and kappa receptors\{\{nl\}\} Blocking opioid receptors would only biologically change something in someone taking an opioid\{\{nl\}\} Used to reverse opioid effects\{\{nl\}\} Can be a diagnostic tool \tn 
% Row Count 21 (+ 12)
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{\emph{naloxone}} & Opioid antagonist used to reverse opioid toxicity (i.e. respiratory depression is the lethal symptom)\{\{nl\}\} Higher affinity for opioid receptors, therefore displaces opioid (competitive antagonist)\{\{nl\}\} No euphoria, no dependence or tolerance\{\{nl\}\}  Schedule II (for emergency purposes only)\{\{nl\}\}Effects = instant withdrawal symptoms: \{\{nl\}\} Pain, hypertension, sweating, anxiety, irritability + (very uncomfortable to patient, but not life-threatening)\{\{nl\}\}  Not a substitute for ambulatory care, but can keep someone alive longer \{\{nl\}\} If opioid agonist is longer acting than naloxone (i.e. methadone), toxicity could return \tn 
% Row Count 53 (+ 32)
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\begin{tabularx}{8.4cm}{x{4 cm} x{4 cm} }
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\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Drug Classes for Pain (cont)}}  \tn
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{\bf{b.Non opioid analgesics}} & Work in peripheral tissues to prevent formation of pain impulses \{\{nl\}\} Most non-opioids are also effective for fever, inflammation, and analgesia \{\{nl\}\} Used for mild or moderate pain associated with inflammation\{\{nl\}\} {\emph{Acetaminophen vs. NSAIDs}}\{\{nl\}\} Acetaminophen does not have anti-inflammatory properties\{\{nl\}\} Both have anti-pyretic and analgesic effects \tn 
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{\emph{Non-steroidal anti-inflammatory drugs\{\{nl\}\}NSAIDs}}\{\{nl\}\}{\emph{Aspirin (ASA), ibuprofen, naproxen (OTC)}} & Primary drugs for the treatment of mild to moderate inflammation\{\{nl\}\} Inhibit cyclo-oxygenase (COX), a key enzyme in the biosynthesis of prostaglandins\{\{nl\}\} Prostaglandins promote inflammation\{\{nl\}\} Reducing prostaglandins effectively reduces inflammation\{\{nl\}\} NSAIDs can be selective for COX-2 or non-selective ALSO anticoagulant, antipyretic, anti-inflammatory\{\{nl\}\} Primary use: for fever, arthritis, mild to moderate musculoskeletal pain, dysmenorrhea\{\{nl\}\} Some drug interactions \{\{nl\}\} Caution in elderly due to poor kidney function\{\{nl\}\} No ASA in children – Reye's Syndrome \tn 
% Row Count 48 (+ 30)
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\begin{tabularx}{8.4cm}{x{4 cm} x{4 cm} }
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\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Drug Classes for Pain (cont)}}  \tn
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{\emph{Acetaminophen}} & Reduce fever at level of hypothalamus and dilation of peripheral blood vessels \{\{nl\}\} Enables sweating and dissipation of heat\{\{nl\}\} Primary use is to relieve mild-moderate pain and reduce fever \{\{nl\}\} No anti-inflammatory actions \tn 
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{\bf{Miscellaneous}} & Focus is the CNS used for neuropathic pain\{\{nl\}\} \tn 
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a.Gabapentin & while shaped similarly to GABA, does not bind to GABA receptors; binds to calcium channels and reduces calcium influx \tn 
% Row Count 21 (+ 6)
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b.Pregabalin (Lyrica®) & reduces calcium influx at nerve terminals, which may reduce transmission of nerve pain \tn 
% Row Count 26 (+ 5)
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{\bf{Corticosteroids}} & Cortisol is released by adrenal glands in response to stimuli to help restore body to normal\{\{nl\}\} Drugs synthetically made to mimic cortisol\{\{nl\}\} They are anti-inflammatory and immuno-suppressive\{\{nl\}\} Primary use: for severe inflammation or immuno-suppression \tn 
% Row Count 40 (+ 14)
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\begin{tabularx}{8.4cm}{x{4 cm} x{4 cm} }
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\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Drug Classes for Pain (cont)}}  \tn
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{\bf{Muscle relaxants}} \{\{nl\}\}{\emph{Methocarbamol, cyclobenzaprine, baclofen, hyoscine}} & After sustaining an injury, muscle spasms may occur to stabilize the affected body part and prevent further damage - also generate pain \{\{nl\}\} Most work in brain to reduce tonic, somatic motor activity in alpha and gamma systems \{\{nl\}\} NOT on muscle cells \{\{nl\}\} NOT at neuromuscular junction \tn 
% Row Count 15 (+ 15)
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{\bf{Anesthetics}} & A drug that causes anesthesia, reversible loss of sensation\{\{nl\}\} Stabilize the neuronal membrane, preventing initiation and conduction of impulses\{\{nl\}\} Primary use is surgery, epidurals\{\{nl\}\}General: a reversible loss of consciousness \{\{nl\}\} Local: a reversible loss of sensation for a limited region of the body while maintaining consciousness \tn 
% Row Count 33 (+ 18)
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\begin{tabularx}{8.4cm}{x{4 cm} x{4 cm} }
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\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Drug Classes for Pain (cont)}}  \tn
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\mymulticolumn{2}{x{8.4cm}}{{\bf{Anti-depressants}}} \tn 
% Row Count 1 (+ 1)
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TCAs & Primary use is depression, moving towards chronic pain\{\{nl\}\} Migraines, nerve pain, fibromyalgia, etc.\{\{nl\}\} Neuropathic pain (due to effect on neurotransmitters) \tn 
% Row Count 10 (+ 9)
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SSRI's \{\{nl\}\}{\emph{Citalopram, fluoxetine, sertraline, paroxetine}} & Selective for serotonin, less side effects than TCAs \{\{nl\}\} Also treat concurrent depression and anxiety disorders\{\{nl\}\} May be effective for chronic fatigue, hot flashes, mostly used off-label for other pathologically similar conditions \tn 
% Row Count 22 (+ 12)
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{\emph{Duloxetine (Cymbalta®) }} & serotonin and norepinephrine reuptake inhibitor\{\{nl\}\} Now indicated for pain associated with diabetic peripheral neuropathy, fibromyalgia, chronic low back pain, and osteoarthritis of the knee\{\{nl\}\} Also depression and generalized anxiety disorder \tn 
% Row Count 35 (+ 13)
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\mymulticolumn{2}{x{8.4cm}}{\bf\textcolor{white}{Drug Classes for Pain (cont)}}  \tn
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{\bf{Anti-anxiety meds}} & {\emph{Benzodiazepines}}\{\{nl\}\} Not a direct MOA, more of a co-morbidity of anxiety along with pain\{\{nl\}\} Worry about tolerance and dependence with long term use\{\{nl\}\} Encourage PRN (as needed) use, other coping mechanisms, counselling \tn 
% Row Count 12 (+ 12)
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\mymulticolumn{2}{x{8.4cm}}{Pain management is subjective and difficult to manage due to consistent change of condition, tolerance, and dependence – and racism \newline Patient is guide to treatment \newline Difficult to know when to encourage more or less use of analgesics}  \tn 
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\end{tabularx}
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% That's all folks
\end{multicols*}

\end{document}